Microenvironment promotes tumor cell reprogramming in human breast cancer cell lines

PLoS One. 2013 Dec 30;8(12):e83770. doi: 10.1371/journal.pone.0083770. eCollection 2013.

Abstract

The microenvironment drives mammary gland development and function, and may influence significantly both malignant behavior and cell growth of mammary cancer cells. By restoring context, and forcing cells to properly interpret native signals from the microenvironment, the cancer cell aberrant behavior can be quelled, and organization re-established. In order to restore functional and morphological differentiation, human mammary MCF-7 and MDA-MB-231 cancer cells were allowed to grow in a culture medium filled with a 10% of the albumen (EW, Egg White) from unfertilized chicken egg. That unique microenvironment behaves akin a 3D culture and induces MCF-7 cells to produce acini and branching duct-like structures, distinctive of mammary gland differentiation. EW-treated MDA-MB-231 cells developed buds of acini and duct-like structures. Both MCF-7 and MDA-MB-231 cells produced β-casein, a key milk component. Furthermore, E-cadherin expression was reactivated in MDA-MB-231 cells, as a consequence of the increased cdh1 expression; meanwhile β-catenin - a key cytoskeleton component - was displaced behind the inner cell membrane. Such modification hinders the epithelial-mesenchymal transition in MDA-MB-231 cells. This differentiating pathway is supported by the contemporary down-regulation of canonical pluripotency markers (Klf4, Nanog). Given that egg-conditioned medium behaves as a 3D-medium, it is likely that cancer phenotype reversion could be ascribed to the changed interactions between cells and their microenvironment.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Breast Neoplasms / pathology*
  • Cadherins / metabolism
  • Caseins / biosynthesis
  • Cell Polarity / drug effects
  • Cell Proliferation / drug effects
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Keratin-18 / metabolism
  • Kruppel-Like Factor 4
  • MCF-7 Cells
  • Mammary Glands, Human / pathology
  • Ovalbumin / pharmacology
  • Protein Transport / drug effects
  • Tumor Microenvironment* / drug effects

Substances

  • ACTA2 protein, human
  • Actins
  • Cadherins
  • Caseins
  • KLF4 protein, human
  • Keratin-18
  • Kruppel-Like Factor 4
  • Ovalbumin

Grants and funding

The present study was partially supported by the Fondazione Roma Terzo Settore (grant no. 8.1.3.3.19.1; URL: http://www.fondazioneroma-terzosettore.it/it/index.html). No additional external funding was received for this study. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.